Effects of antioxidants on oxidative stress and inflammatory responses of human bronchial epithelial cells exposed to particulate matter and cigarette smoke extract

• Published in: Toxicology in vitro 2020-09, Vol.67, p.104883, Article 104883
• Main Authors: Son, Eun Suk, Park, Jeong-Woong, Kim, Yu Jin, Jeong, Sung Hwan, Hong, Jeong Hee, Kim, Se-Hee, Kyung, Sun Young
• Format: Article
• Language: English
• Subjects: Acetylcysteine; Acetylcysteine - pharmacology; Air pollution; Antioxidants; Antioxidants - pharmacology; Bronchi - cytology; Cell Line; Cell Survival - drug effects; Chronic obstructive pulmonary disease; Cigarette smoke; Cigarette smoke extract; COPD; Cytokines; Cytokines - genetics; Cytotoxicity; Epithelial cells; Epithelial Cells - drug effects; Epithelial Cells - metabolism; Exposure; Gene expression; Health risks; Humans; Inflammation; Isothiocyanates - pharmacology; Lung diseases; MAP kinase; NF-E2-Related Factor 2 - metabolism; Obstructive lung disease; Oxidative stress; Oxidative Stress - drug effects; Particulate emissions; Particulate matter; Particulate Matter - toxicity; Pollutants; Reactive Oxygen Species - metabolism; Signal transduction; Signaling; Smoke; Sulforaphane; Sulforaphane N-acetyl-L-cysteine; Tobacco Products; Toxicity
• ISSN: 0887-2333; 1879-3177
• DOI: 10.1016/j.tiv.2020.104883

Particulate matter (PM) is a type of air pollutant that induces adverse health effects, including acute exacerbation of chronic obstructive pulmonary disease (COPD). However, the effects of co-exposure to PM and cigarette smoke extract (CSE) on bronchial epithelial cells remain unknown. This study investigated the cytotoxic and pro-inflammatory effects of combined exposure to PM and CSE on bronchial epithelial cells, and assessed the potential of antioxidants to inhibit CSE/PM-induced oxidative stress and inflammation. Exposure of epithelial cells to PM or CSE induced cytotoxicity, inflammation, and oxidative stress, all of which were dramatically increased when cells were exposed to the combination of CSE and PM. Importantly, the adverse effects of CSE/PM exposure were suppressed when cells were treated with sulforaphane (SFN) or sulforaphane N-acetylcysteine (SFNAC). Furthermore, SFN and SFNAC suppressed the CSE/PM-induced pro-inflammatory cytokine production and expression of inflammatory genes. Combined PM and CSE exposure further activated the MAPK and Nrf2 signaling pathways. SFN and SFNAC attenuated CSE/PM-induced epithelial toxicity through the ERK/JNK signaling pathway-dependent inhibition of inflammation. Moreover, SFN and SFNAC suppressed ROS generation by activating antioxidant enzymes and Nrf2 signaling. Therefore, SFN and SFNAC could be a promising approach to prevent or mitigate the exacerbation of pulmonary diseases caused by PM and other air pollutants. •PM aggravates CSE-induced oxidative stress and inflammation in bronchial epithelial cells.•SFN and SFNAC attenuated CSE/PM-induced epithelial cell toxicity through the MAPK/Nrf2 signaling pathways.•Antioxidants may have a therapeutic potential in PM-induced acute exacerbation of chronic pulmonary diseases.